Unknotting reciprocal causation between organism and environment

In recent years, biologists and philosophers of science have argued that evolutionary theory should incorporate more seriously the idea of ‘reciprocal causation.’ This notion refers to feedback loops whereby organisms change their experiences of the environment or alter the physical properties of their surroundings. In these loops, in particular niche constructing activities are central, since they may alter selection pressures acting on organisms, and thus affect their evolutionary trajectories. This paper discusses long-standing problems that emerge when studying such reciprocal causal processes between organisms and environments. By comparing past approaches to reciprocal causation from the early twentieth century with contemporary ones in niche construction theory, we identify two central reoccurring problems: All of these approaches have not been able to provide a conceptual framework that allows (i) maintaining meaningful boundaries between organisms and environments, instead of merging the two, and (ii) integrating experiential and physical kinds of reciprocal causation. By building on case studies of niche construction research, we provide a model that is able to solve these two problems. It allows distinguishing between mutually interacting organisms and environments in complex scenarios, as well as integrating various forms of experiential and physical niche construction.

Reciprocal causation mixture model for robust mendelian randomization analysis using genome-scale summary data

Mendelian randomization (MR) using GWAS summary statistics has become a popular method to infer causal relationships across complex diseases. However, the widespread pleiotropy observed in GWAS has made the selection of valid instrumental variables (IVs) problematic, leading to possible violations of MR assumptions and thus potentially invalid inferences concerning causation. Furthermore, current MR methods can examine causation in only one direction, so that two separate analyses are required for bi-directional analysis. In this study, we propose a novel strategy, MRCI (Mixture model Reciprocal Causation Inference), to estimate reciprocal causation between two phenotypes simultaneously using the genome-scale summary statistics of the two phenotypes and reference linkage disequilibrium (LD) information. Simulation studies, including strong correlated pleiotropy, showed that MRCI obtained nearly unbiased estimates of causation in both directions, and correct Type I error rates under the null hypothesis. In applications to real GWAS data, MRCI detected significant bi-directional and uni-directional causal influences between common diseases and putative risk factors.

Cultural Change through the Interplay between Actors and Environments: Niche Construction and a Multilevel Approach

Researchers theorize cultural change as societal adaptation to the environment. However, the ecological framework typically ignores the fact that people systematically create their own environment, effectively changing the ecology to which they adapt. Here we advance conceptual and analytical tools for a more dynamic framework of cultural change. First, we draw on the theory of niche construction to argue that organisms modify their environments in ways that impact their own evolution. Second, we advocate for a multilevel approach to analyze heterogeneity of longitudinal processes across multiple units: cultural change can be understood as a within-society process nested within higher-level units that differ across space. We then apply a distributed lag/lead model, which owes to multilevel modeling, to identify the mutual causality between environment and culture. Focusing on the 50 U.S. states, we analyzed how modernization variables—wealth and individualism—functioned to reduce tuberculosis (TB, 1993-2018) and sexually transmitted diseases (STD, 1984-2014). We found evidence for reciprocal causation: modernization generally preceded reduction of TB and STD, but decrease in these diseases also increased future wealth and individualism. Moreover, the positive impacts of modernization on mitigating future diseases were stronger among collectivistic states, especially for the relationship between rising individualism and reduction of STD. We explore the virtues and limitations of this approach, but encourage a more dynamic approach in research on cultural change.

Enhancing Adherence to Voice Therapy via Social Cognitive Strategies

Treatment adherence is a challenge in behavioral voice therapy. Patients commonly encounter difficulties with practicing and implementing target voice techniques outside of the clinic. Several mobile support strategies have been shown to improve adherence. These strategies are driven by social cognitive theory, which provides a theoretical but practical framework for understanding adherence behavior and solving adherence problems. Key features of the theory include (1) its model of triadic asymmetrical reciprocal causation, (2) the concept of human agency, and (3) the constructs of self-efficacy and goal commitment. The purpose of this article is to (1) explain voice therapy adherence within the framework of social cognitive theory, (2) illustrate three broad categories of adherence problems, and (3) provide examples of strategies to address each. With this exemplified knowledge, the clinician can diagnose factors that underlie patients' adherence problems and develop individualized solutions. Given the significant role adherence plays in behavioral interventions, this information holds substantial clinical relevance.

HFD and HFD-provoked hepatic hypoxia act as reciprocal causation for NAFLD via HIF-independent signaling

Background The occurrence of non-alcoholic fatty liver disease (NAFLD) is found to be higher in patients with obstructive sleep apnea (OSA), which is characterized by intermittent hypoxia. Activation of hypoxia-inducible factors has been shown in the development and progression of NAFLD, implying a cause and effects relationship between NAFLD and hypoxia. The present study was designed to investigate the interaction of lipotoxicity and hypoxia in the pathogenesis of NAFLD using mice model with high-fat diet (HFD) feeding or hypoxic treatment. Methods NAFLD model was induced in mice by HFD feeding, and in cultured primary hepatocytes by administration of palmitate acid. Mouse hypoxic model was produced by placing the mice in a Animal incubator with oxygen concentration at 75% followed by a 21% oxygen supplement. Hypoxic condition was mimicked by treating the hepatocytes with cobalt chloride (CoCl2) or 1% oxygen supply. Pimonidazole assay was conducted to evaluate hypoxia. Lipid metabolic genes were measured by real-time polymerase-chain reaction. HIF-1α and HIF-2α genes were silenced by siRNA. Results HFD feeding and palmitate acid treatment provoked severe hepatic hypoxia along with TG accumulation in mice and in cultured primary hepatocytes respectively. Conversely, hypoxia induced hepatic TG accumulation in mice and in cultured primary hepatocytes. Hypoxic treatment inhibited the expression of lipolytic genes, while increased the expression of lipogenicgenes in mice. Although both lipotoxicity and hypoxia could activate hepatic hypoxia-induced factor 1α and 2α, while neither lipotoxicity- nor hypoxia- induced hepatic steatosis was affected when HIF was knocked down. Conclusions HFD resulted in hepatic TG accumulation and concomitant hypoxia. Conversely, hypoxia induced hepatic TG accumulation in mice and in cultured heptocytes. Thus lipotoxicity and hypoxia might work as reciprocal causation and orchestrate to promote the development of NAFLD.

The Reciprocal Causation of the Eucharist and the Church: A Critical Analysis from Catholic Theological Perspective

The Catholic Church believes in the intrinsic and inseparable bond of the Holy Eucharist and the Church. In reference to its dogmatic Constitution, Lumen Gentium paragraph 11 (LG 11) the Church professes that the Eucharist, which is the body and blood of Jesus Christ, is “the source and summit of Christian life.” Each of these two sacraments effects and builds each other. This implies that as the church celebrates the Eucharist, the members as they partake in the Holy Communion manifest concretely their unity and become one body of Christ. This article seeks to underscore the indissoluble reciprocal causality of the Eucharist and the Church, while it stresses on the Eucharist as the origin, the being, and the destiny of the Church. The study drums home critically the idea that the Eucharist builds the Church, and the Church makes the Eucharist. These are but two complementary terms, the Body of Christ, the Church which lives and continuously builds itself up through the Eucharist, Body of Christ. This great theological theme is one of the central points of a deeper interest in Orthodox, Roman Catholic and Anglican ecclesiology. However, the paper examines critically the reciprocal causality between the Church and the Eucharist from the Catholic perspective as proposed by H. de Lubac, a French theologian. It finally treats the interpenetration of the Eucharist as the Body of Christ and the Church as the Body of Christ from the perspective of sacramental theology.

The ATP Hypothesis: A New Conceptual Framework for the Origin of the Genetic Code

More than half a century has passed since the discovery of the genetic code, but its origin is still one of the greatest mysteries in life science, although a plenty of theories have been proposed so far, as none can explain satisfactorily why the genetic code evolved in such a way, especially in the context of the biochemical system, a relation of part to whole. Here, a new hypothesis is proposed, according to which ATP is at the origin of the genetic code by its coevolution with the pristine biochemical system of the protocell. This hypothesis shows how primitive life with its genetic code emerged through a series of processes from energy flow to information communication mediated by ATP. First, ATP is the only energetic product of photosynthesis, and is at the energetic heart of the extant biochemical systems. Second, ATP serves as not only an energy carrier but also an informatization molecule, as ATP could energetically elongate chains of both polynucleotides and polypeptides, thus providing a bridge between these molecules and eventually mediating biochemical innovation in the protocell from energy transformation to informatization, a process for creating and managing information. Informatization was inevitably coupled with structuralization (processes for organizing or incorporating cellular structures), cyclizing polynucleotides and polypeptides into a feedback loop of reciprocal causation. The triplet codon might be only for stereochemical handling of amino acids through, e.g., Watson–Crick pairing interactions. It is only the evolutionary completion of the genetic code from RNA to DNA that, contrary to the central dogma, marked the dawn of cellular life, when Darwinian evolution began to operate. The ATP hypothesis sheds light on the origin of life, together with the formation of both photosynthetic and biochemical systems, which remains largely unknown thus far.